Mechanisms of Aspirin Desensitization - 30/04/13

Doi : 10.1016/j.iac.2012.11.003

Trever Burnett, MD ^a, Rohit Katial, MD ^b,^⁎ , Rafeul Alam, MD, PhD ^c
^a Adult Program, Department of Allergy and Immunology, National Jewish Medical and Research Center, University of Colorado, 1400 Jackson Street, K624, Denver, CO 80206, USA
^b Weinberg Clinical Research Unit, Adult Fellowship Program, Department of Allergy and Immunology, National Jewish Medical and Research Center, University of Colorado, 1400 Jackson Street, K624, Denver, CO 80206, USA
^c Division of Allergy and Immunology, National Jewish Medical and Research Center, University of Colorado, 1400 Jackson Street, K624, Denver, CO 80206, USA

Corresponding author.

Résumé

Aspirin-exacerbated respiratory disease is a clinical syndrome characterized by severe, persistent asthma, hyperplastic eosinophilic sinusitis with nasal polyps, and reactions to aspirin and other nonsteroidal antiinflammatory drugs that preferentially inhibit cyclooxygenase 1. The mechanisms behind the therapeutic effects of aspirin desensitization remain poorly understood. Recent studies suggest that the clinical benefits may occur through direct inhibition of tyrosine kinases and the signal transducer and activator of transcription 6 signaling pathway, which results in inhibition of interleukin 4 production. In this article, the current understanding of the mechanisms of aspirin desensitization is reviewed and future areas of investigation are discussed.

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Keywords : Aspirin-exacerbated respiratory disease (AERD), Aspirin desensitization, Mechanisms of action, Cysteinyl leukotrienes (CysLTs), Cytokines, Interleukin 4 (IL-4), Signal transducer and activator of transcription 6 (STAT6)